Spatial metrics to study urban patterns in growing and shrinking cities

This article reviews existing literature on spatial metrics, presenting a portfolio of metrics addressing the spatial patterns of growing and shrinking cities and discussing their potential and limitations. A wide and diverse set of spatial metrics was found. While these metrics address most of the identified spatial patterns of urban growth, spatial metrics used in urban shrinkage studies are much scarcer and not nearly sufficient to provide a comprehensive assessment of its spatial patterns. The article concludes that there is great potential for the development of new spatial metrics or mixed indicators, particularly in shrinkage contexts. The article builds on recent literature focusing on reviewing and developing metrics for particular spatial patterns (notably patterns of urban sprawl), while considering a very broad and multidisciplinary set of metrics. It focuses not only on the outcomes of urban growth but also on those of the increasingly common shrinking phenomenon.This research was funded by the Portuguese Foundation for Science and Technology (SFRH/BD/71970/2010), co-financed by the European Social Fund through the POPH Programme.This is the author accepted manuscript. The final version is available from Taylor & Francis via http://dx.doi.org/10.1080/02723638.2015.109611

Caso para diagnóstico

Human scabies is an intensely pruritic skin infestation caused by Sarcoptes scabiei var. hominis. Crusted scabies (previously known as Norwegian scabies) is a rare form, very contagious and transmitted by direct contact with the skin. Despite being readily treatable, a delayed diagnosis often leads to widespread infestation of contacts, and therefore difficult to restrain. This case concerns a patient where dermoscopy (with scabetic burrows and a visible hand-glider structure), together with direct microscopic examination, allowed a prompt diagnosis, thereby reinforcing the increasing importance of this technique in daily practice

Lower Extremity Burns with Bone Exposure: Reconstruction with Dermal Regeneration Template

Introdução: As soluções reconstrutivas das queimaduras dos membros inferiores com exposição óssea (transferência de tecidos vascularizados) e dos defeitos do escalpe, não susceptíveis de encerramento com retalhos locais (expansão tecidual), são complexas, morosas e, por vezes, inviáveis. O recurso a substitutos cutâneos biológicos, como a matriz de regeneração dérmica, constitui uma importante alternativa às soluções reconstrutivas tradicionais. Relato dos casos: Estudo retrospectivo de 246 doentes com queimaduras dos membros inferiores, admitidos na Unidade de Queimados/Serviço de Cirurgia Plástica do nosso Centro Hospitalar, entre Janeiro de 2007 e Dezembro de 2008. Os autores apresentam 2 casos clínicos com queimaduras bilaterais das pernas e com exposição óssea. Nos dois casos, realizou-se desbridamento tangencial e encerramento das áreas cruentas com um substituto cutâneo, a matriz de regeneração dérmica. Na 4ª semana após a aplicação da matriz, o componente externo da membrana bilaminar foi substituído por enxerto de pele parcial. Obteve-se cobertura estável das áreas cruentas, sem necessidade de procedimentos cirúrgicos adicionais. Conclusões: A utilização de substitutos dérmicos expande as opções reconstrutivas nos casos de queimaduras com exposição óssea dos membros inferiores. A utilização da matriz biológica permitiu a preservação dos membros nos dois pacientes. A matriz de regeneração dérmica possibilitou uma cobertura estável de estruturas vitais, sem necessidade de transferência ou expansão tecidual e com morbilidade mínima

Paraneoplastic pemphigus with clinical features of lichen planus associated with low-grade B cell lymphoma

BACKGROUND: Neoplasia-induced lichen planus is described as a cell-mediated reaction to unknown epithelial antigens. Paraneoplastic pemphigus (PNP), characterized by the presence of a specific array of autoantibodies, probably represents a different form of presentation of the same autoimmune syndrome where the mucocutaneous expression depends on the dominant pathologic mechanism. METHODS: The authors report a case of PNP with predominant lichen planus-like lesions and review the relevant literature. We observed a 74-year-old female with vesico-bullous, erosive, target-shaped and flat papular lichenoid lesions on the lower legs, palms and soles, evolving for 3 weeks. Histopathology revealed a lichenoid dermatitis. Direct immunofluorescence showed C3 deposition around keratinocytes and epidermal IgG intranuclear deposition. Indirect immunofluorescence revealed circulating IgG with intercellular staining on rat bladder substrate. Immunoblotting demonstrated bands of 130, 190, 210 and 250 kDa antigens. A pararenal B cell lymphoma was found. RESULTS: Oral corticotherapy with 40 mg prednisolone daily was initiated with a good cutaneous response. Four months later, cyclophosphamide (50 mg/day) was introduced because of a discrete enlargement of the pararenal mass. The patient died on the seventh month of follow up as a result of respiratory insufficiency. CONCLUSION: PNP has different forms of presentation and the lack of a consensus about diagnostic criteria may contribute to underdiagnosed cases. Advances on the knowledge of the sensitivity and specificity of diagnostic criteria have allowed a better accuracy of diagnosis

Myosin II synergizes with F-actin to promote DNGR-1-dependent cross-presentation of dead cell-associated antigens

Conventional type 1 DCs (cDC1s) excel at cross-presentation of dead cell-associated antigens partly because they express DNGR-1, a receptor that recognizes exposed actin filaments on dead cells. In vitro polymerized F-actin can be used as a synthetic ligand for DNGR-1. However, cellular F-actin is decorated with actin-binding proteins, which could affect DNGR-1 recognition. Here, we demonstrate that myosin II, an F-actin-associated motor protein, greatly potentiates the binding of DNGR-1 to F-actin. Latex beads coated with F-actin and myosin II are taken up by DNGR-1+ cDC1s, and antigen associated with those beads is efficiently cross-presented to CD8+ T cells. Myosin II-deficient necrotic cells are impaired in their ability to stimulate DNGR-1 or to serve as substrates for cDC1 cross-presentation to CD8+ T cells. These results provide insights into the nature of the DNGR-1 ligand and have implications for understanding immune responses to cell-associated antigens and for vaccine design

Broadening Risk Factor or Disease Definition as a Driver for Overdiagnosis: A Narrative Review

Medical overuse-defined as the provision of health services for which potential harms exceed potential benefits-constitutes a paradigm of low-value care and is seen as a threat to the quality of care. Value in healthcare implies a precise definition of disease. However, defining a disease may not be straightforward since clinical data do not show discrete boundaries, calling for some clinical judgment. And, if in time a redefinition of disease is needed, it is important to recognize that it can induce overdiagnosis, the identification of medical conditions that would, otherwise, never cause any significant symptoms or lead to clinical harm. A classic example is the impact of recommendations from professional societies in the late 1990s, lowering the threshold for abnormal total cholesterol from 240 mg/dl to 200 mg/dl. Due to these changes in risk factor definition, literally overnight there were 42 million new cases eligible for treatment in the United States. The same happened with hypertension-using either the 2019 NICE guidelines or the 2018 ESC/ECC guidelines criteria for arterial hypertension, the proportion of people overdiagnosed with hypertension was calculated to be between 14% and 33%. In this review, we will start by discussing resource overuse. We then present the basis for disease definition and its conceptual problems. Finally, we will discuss the impact of changing risk factor/disease definitions in the prevalence of disease and its consequences in overdiagnosis and overtreatment (a problem particularly relevant when definitions are widened to include earlier or milder disease).info:eu-repo/semantics/publishedVersio

Immunoglobulin genes implicated in glioma risk

Both genetic and environmental factors are thought to be causal in gliomagenesis. Several genes have been implicated in glioma development, but the putative role of a major immunity-related gene complex member, immunoglobulin heavy chain γ (IGHG) has not been evaluated. Prior observations that IGHG-encoded γ marker (GM) allotypes exhibit differential sensitivity to an immunoevasion strategy of cytomegalovirus, a pathogen implicated as a promoter of gliomagenesis, has lead us to hypothesize that these determinants are risk factors for glioma. To test this hypothesis, we genotyped the IGHG locus comprising the GM alleles, specifically GM alleles 3 and 17, of 120 glioma patients and 133 controls via TaqMan® genotyping assay. To assess the associations between GM genotypes and the risk of glioma, we applied an unconditional multivariate logistic regression analysis adjusted for potential confounding variables. In comparison to subjects who were homozygous for the GM 17 allele, the GM 3 homozygotes were over twice as likely, and the GM 3/17 heterozygotes were over three times as likely, to develop glioma. Similar results were achieved when analyzed by combining the data corresponding to alleles GM 3 and GM 3/17 in a dominant model. The GM 3/17 genotype and the combination of GM 3 and GM 3/17 were found to be further associated with over 3 times increased risk for high-grade astrocytoma (grades III-IV). Allele frequency analyses also showed an increased risk for gliomas and high-grade astrocytoma in association with GM 3. Our findings support the premise that the GM 3 allele may present risk for the development of glioma, possibly by modulating immunity to cytomegalovirus

Broadening Risk Factor or Disease Definition as a Driver for Overdiagnosis: A Narrative Review

Medical overuse-defined as the provision of health services for which potential harms exceed potential benefits-constitutes a paradigm of low-value care and is seen as a threat to the quality of care. Value in healthcare implies a precise definition of disease. However, defining a disease may not be straightforward since clinical data do not show discrete boundaries, calling for some clinical judgment. And, if in time a redefinition of disease is needed, it is important to recognize that it can induce overdiagnosis, the identification of medical conditions that would, otherwise, never cause any significant symptoms or lead to clinical harm. A classic example is the impact of recommendations from professional societies in the late 1990s, lowering the threshold for abnormal total cholesterol from 240 mg/dl to 200 mg/dl. Due to these changes in risk factor definition, literally overnight there were 42 million new cases eligible for treatment in the United States. The same happened with hypertension-using either the 2019 NICE guidelines or the 2018 ESC/ECC guidelines criteria for arterial hypertension, the proportion of people overdiagnosed with hypertension was calculated to be between 14% and 33%. In this review, we will start by discussing resource overuse. We then present the basis for disease definition and its conceptual problems. Finally, we will discuss the impact of changing risk factor/disease definitions in the prevalence of disease and its consequences in overdiagnosis and overtreatment (a problem particularly relevant when definitions are widened to include earlier or milder disease).info:eu-repo/semantics/publishedVersio